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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Micropuncture and morphologic studies were performed in six groups of male Munich-Wistar rats after removal of the right kidney and segmental infarction of two-thirds of the left kidney. Groups 1 and 4 received no specific therapy. Groups 2 and 5 were treated with the angiotensin I-converting enzyme inhibitor, enalapril, 50 mg/liter, in the drinking water. Groups 3 and 6 were treated with reserpine (5 mg/liter), hydralazine (80 mg/liter), and hydrochlorothiazide (25 mg/liter). All rats were fed standard chow. Groups 1-3 underwent micropuncture study 4 wk after renal ablation. Untreated group 1 rats exhibited systemic hypertension and elevation of the single nephron glomerular filtration rate (SNGFR) due to high average values for the mean glomerular transcapillary hydraulic pressure gradient (delta P) and glomerular plasma flow rate (QA). In group 2 rats, treatment with enalapril prevented systemic hypertension and maintained delta P at near-normal levels without significant reduction in SNGFR and QA. In contrast, triple drug therapy normalized systemic hypertension, but failed to lower delta P in group 3 rats. Groups 4-6 were followed for 12 wk after renal ablation. Untreated group 4 rats demonstrated continuous systemic hypertension, progressive proteinuria, and glomerular structural lesions, including mesangial expansion and frequent areas of segmental sclerosis. In group 5 rats, treatment with enalapril maintained systemic blood pressure at normal levels over the 12-wk period and dramatically limited the development of proteinuria and glomerular lesions. Despite equivalent systemic blood pressure control in group 6 rats, failure of triple drug therapy to control glomerular hypertension was associated with progressive proteinuria and glomerular lesions comparable to those seen in untreated group 4 rats. Thus, unless glomerular capillary hypertension is corrected, control of systemic blood pressure is insufficient to prevent progressive renal injury in rats with reduced renal mass.
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PMID:Therapeutic advantage of converting enzyme inhibitors in arresting progressive renal disease associated with systemic hypertension in the rat. 301 63

Micropuncture and morphological studies were performed in three protocols assessing the renal hemodynamic and structural effects of angiotensin I-converting enzyme inhibitors (CEIs) in the progression of glomerular injury. In protocol I, rats were subjected to 5/6 renal ablation and received no therapy, enalapril (CEI), or triple-drug therapy (TRX) for 12 weeks. Control of systemic and glomerular hypertension with CEI resulted in prevention of glomerular capillary hypertension and protection against glomerular injury. Despite equivalent control of systemic BP, failure of TRX to control glomerular hypertension was associated with no protection against eventual proteinuria and glomerular sclerosis, values for these indexes being as abnormal as in rats receiving no therapy. In protocol II, rats were again subjected to 5/6 renal ablation and followed for 18 weeks. Early institution of CEI soon after ablation again prevented systemic and glomerular hypertension and largely limited glomerular injury. In a third group, enalapril therapy was delayed for 8 weeks after ablation until hypertension and proteinuria were established. Late institution of CEI resulted in prompt reduction in systemic and glomerular capillary hypertension and stabilization of glomerular disease. In protocol III, CEI was administered to normotensive, moderately hyperglycemic diabetic rats. A modest, 20-mm Hg reduction in systemic arterial pressure was associated with the normalization of glomerular capillary pressure and a striking reduction in the development of albuminuria and glomerular injury. These studies suggest that CEI effectively prevent glomerular capillary hypertension and thereby afford protection against glomerular injury in diverse models of progressive renal disease.
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PMID:Therapeutic implications of converting-enzyme inhibitors in renal disease. 303 94

Because of the advance of techniques and age-matched apparatus for blood pressure measurement, and because of the availability of age-related normal values in childhood, the knowledge of the number of children having elevated blood pressures has recently improved. In a group of healthy children, the first important task is to determine how many incidences of "essential hypertension" there are among them, which may appear in childhood and persist into adulthood. This should urge us to undertake periodical examinations of healthy children. On the other hand, the treatment of "secondary hypertension" has similarly been improved. Since 1979 in particular, captopril, an orally active angiotensin I-converting enzyme inhibitor, has successfully been administered to treat children with malignant hypertension and who respond poorly to conventional antihypertensive therapies. We report 3 cases that received captopril for refractory hypertension: a 2-year-old boy with renal and renovascular anomalies, a 7-year-old boy with moyamoya disease after surgical operation, and a 17-year-old youth with Cushingoid syndrome due to chronic administration of steroids against mixed connective tissue disease. After the introduction of captopril, good pressure control was obtained in all 3 cases, although reasonable effects of measurement values of the renin-angiotensin-aldosterone system (decrease in angiotensin I & II, increase in I/II ratio, etc.) were found only in the first case.
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PMID:Refractory hypertension in childhood--efficacy of captopril therapy. 332 1

To determine whether chronic antihypertensive therapy prevents the progression of cardiac hypertrophy and the deterioration in cardiac performance observed in spontaneously hypertensive rats (SHR) with long-term hypertension, 14-month-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 months with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/liter of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-month-old SHR (untreated, 4.37 +/- 0.2 mg/g of body weight; treated, 3.01 +/- 0.1 mg/g; P less than 0.02) to levels observed in 6-month-old SHR. Treatment prevented the reductions in baseline and maximal aortic blood flows that occurred in SHR between ages 12 and 24 months yet had no effect on the blood flows of NWR. The diminished maximal stroke volume of untreated SHR was ejected from a significantly increased left ventricular end-diastolic volume, so that the ejection-fraction index was markedly reduced (24-month-old untreated NWR, 84 +/- 3%; untreated SHR, 56 +/- 5%; P less than 0.001). Therapy restores this index in SHR to normal (77 +/- 4%). The relationship between ejection-fraction index, and afterload was also normal in treated SHR. Thus, chronic therapy with captopril produced a marked regression of cardiac hypertrophy and prevented the deterioration of cardiac performance in SHR with long-standing hypertension.
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PMID:Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the spontaneously hypertensive rat. 621 29

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.
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PMID:[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)]. 627 8

Five children with high-renin hypertension unresponsive to conventional medications were effectively treated with the angiotensin I-converting enzyme inhibitor, captopril, for six to 26 months. Age groups included children 6 to 13 years old and a 33-week gestation preterm infant with hypertension related to umbilical artery catheterization. Significant adverse reactions were limited to transient renal insufficiency in the preterm infant and increased azotemia in an older child with chronic renal failure.
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PMID:Captopril. Long-term treatment of hypertension in a preterm infant and in older children. 633 72

In low-renin hypertensive patients, the acute effect of the angiotensin I-converting enzyme inhibitor, captopril, was evaluated in relation to the response of plasma bradykinin (PBK) levels as a parameter of its inhibitory effect on kininase II. Captopril significantly lowered the blood pressure and increased PBK levels. While there was no significant relationship between the reduction of blood pressure and pretreatment plasma renin activity, a significant correlation was observed between the antihypertensive effect of captopril and changes in PBK (r = -0.834, p less than 0.01, n = 10). Furthermore, in a patient with primary aldosteronism and, also, in a patient with glucocorticoid responsive hyperaldosteronism, captopril increased plasma PBK with reduction of the blood pressure. It is likely, therefore, that in low-renin hypertension, the vasodepressor effect of acute converting enzyme inhibition is due mainly to kinin accumulation rather than inhibition of angiotensin II formation.
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PMID:Evidence for the role of kinins in the acute antihypertensive effect of captopril in low-renin hypertension. 638 85

Cultured JGC contain renin, angiotensin I, angiotensin I-converting enzyme, angiotensin II, and, by implication, the entire RAS. JGC, as transplants, appear to secrete angiotensin II/III directly into the bloodstream to cause hypertension when the renal mass is reduced. There are two main phases of the hypertensive state, an angiotensin-dependent developmental phase and a non-angiotensin-dependent maintenance phase. This model may be useful in attempts to evaluate pro-hypertensive actions of angiotensin other than those due to direct systemic vasoconstriction. Certain of these actions appear to be intrarenal and include the stimulation of sodium reabsorption, a decrease in renopapillary blood flow, the stimulation of prostaglandin synthesis, and a constraint on the antihypertensive function of the RIC.
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PMID:Cultured juxtaglomerular cells cause hypertension by secreting angiotensin. 676 10

The role of endogenous prostaglandins in the antihypertensive mechanism of orally active angiotensin I-converting enzyme inhibitor in low renin hypertension was investigated. In the SQ 14225-responders with low renin hypertension, blood pressure was elevated to control level and antihypertensive effect of SQ 14225 was attenuated after the inhibition of endogenous prostaglandin synthesis with indomethacin, while no significant change in blood pressure was found in the SQ 14225-responders with normal renin hypertension. Urinary prostaglandin E excretion was not significantly increased after the SQ 14225 administration but significantly decreased after the administration of indomethacin. There was no significant difference in urinary prostaglandin E excretion between normal renin hypertension and low renin hypertension. These results suggest that SQ 14225 may potentiate extrarenal vasodilating prostaglandin system, probably vascular prostaglandin system, contributing to the antihypertensive mechanism in SQ 14225-responders with low renin hypertension. The augmented renin release following SQ 14225 administration was inhibited by indomethacin, suggesting that endogenous prostaglandin system may contribute to the negative short feedback mechanism of renin release.
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PMID:Implication of endogenous prostaglandin system in the antihypertensive effect of captopril, SQ 14225, in low renin hypertension. 699 21

A convincing response to the orally administered angiotensin I-converting enzyme inhibitor captopril (SQ 14225) in a severe hyper-reninaemic hypertensive patient resistant to other forms of treatment is described. The use of this drug in accelerated severe hypertension with impending organ damage is suggested during the early phase of treatment.
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PMID:Response of malignant hypertension with refractory cardiac failure to captopril: A case report. 699 55


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